How to Treat Peripartum Acute Renal Failure, Cardiorenal and Renocardiac Syndromes - Case Study Example

CASE STUDY This case study involves a 20 years old woman who was found at a shopping mall unconscious. The F2 who saw her in A/E found her to be comatose with laboured breathing, an offensive smelling breath and with numerous small infected cuts on her hands. She ordered laboratory tests for both blood and urine samples. The results were as follows; Blood specimen A, Serum sodium 139mmol/L was found to be normal, Serum potassium 6.0mmol/L was elevated, Serum creatinine 97 µmol/L was assumed to be higher because her baseline was not known at the time of these tests, Urea 15mmol/L was found to be higher in the blood serum. Blood specimen B Haemoglobin 12.8g/dL was normal, total white cell count 14.0 x10^9L was elevated indication of an infection, Platelets 266 x10^9L /L, were of normal level. Urine Examination was pH: 5, there was no protein detection, bilirubin, and blood, urobilinogen not excess, white and red cells turned out negative. These results were interpreted to mean that she was suffering from acute kidney injury, while the presence of glucose and ketones was assumed to be an indication of diabetes nephropathy and the observation of the presence of crystals of calcium oxalate in the urine sample was an indicative of kidney obstruction or kidney stones. WHAT DO THE TEST RESULTS REVEAL ABOUT THIS YOUNG WOMAN’S PRESENT CONDITION? The analysis of the test result reveals that she was suffering of acute kidney injury, because of the single raise of serum creatinine, which was without a baseline serum creatinine measurement though more assessment needs to be done to confirm this. The accumulation or urea in the blood serum above the recommended level with excretion of calcium oxalate crystals in the urine indicates that she is having some kind of renal obstruction, which is either caused by kidney stones or fibrosis. Therefore, with this in mind assumed that she had an acute kidney injury. Though it is recommended that she continuous to be monitored to assess the rate of declining of creatinine level in the blood and this should be done within two weeks. Where acute decline is suspected and the clinical picture indicates concurrent illness the creatinine should be repeated within 24 hours. (National Institute for Health and Clinical Excellence (NICE) 2008) Upon admonition her urine was analyzed and it was found to be negative for blood and protein indicating a reduced renal blood flow and urinary tract obstruction because of the presence of calcium oxalate. (Brincat and Hilton 2008) the urinalysis indicated the presence of calcium oxalate, which was an indicative of urinary tract stones or malignancy. Because of the presence of high concentration of serum potassium > 6.0 mmol/L. suggests that she has a acute kidney failure (Bellomo et al 2012) the laboratory results suggests that she is suffering from post-renal injury, which was caused by calcium oxalate a blockage to urine flow, resulting in a back pressure to the kidney, causing damage to nephrons. This is obstructive nephropathy and is a relatively uncommon cause of acute kidney injury (5%). Timely diagnosis and treatment can lead to a complete recovery. The most frequent causes of obstructive nephropathy include: (Hilton 2006) HOW DOES THE TEST RESULTS EXPLAIN HER LOSS OF CONSCIOUSNESS Her unconsciousness would be as a result of reduced effective circulating volume of blood due to the accumulation of blood under the skin, as the presence of serum potassium indicates. Also antidiuretic hormone released results in increased distal water and urea reabsorption this explain why she has abnormal level of urea in the blood serum. There was electrolytes such as sodium, potassium, uric acid accumulation in her blood during acute kidney injury, because of these she experienced unconsciousness, coma, and due to oedema of the lungs she was breathlessness and cause life-threatening complications, such as cardiac arrest. (Bellomo et al 2012) WHAT DO YOU CONCLUDE HER DIAGNOSIS TO BE BASED ON YOUR UNDERSTANDING OF THE RESULTS ABOVE The conclusion of her diagnosis was based on the fact that acute kidney failure is characterized by a rapid, decline fall in glomerular filtration rate and retention of nitrogenous waste products over a period of hours or days. It is classified into pre-renal, renal (intrinsic) and post-renal failure. (Segheb et al 2008) Post-renal ARF follows obstruction of the urinary collection system with an increase in pressure within the renal collecting systems resulting in reduced GFR and renal failure. (Lameire at el 2006) The absence of blood, bilirubin, urobilinogen, white, and red cells and protein in the urine was most compatible with prerenal or postrenal acute kidney injury. The presence of crystals of calcium oxalate in the urine, which might have been as a result of ethylene glycol poisoning, methoxyflurane toxicity, crystalluria in an AIDS patient due to use of acyclovir or indinavir indicative of acute kidney injury. (Kanbay et al 2009) According to Hu and group, she may have experienced obstructive nephropathy, which is a major cause of renal dysfunction among children and adults. The oxalate or kidney stones obstruction nephropathy, the morphological lesions in the obstructed kidney are characterized by peritubular capillaries rarefaction, tubular atrophy, inflammatory infiltration, widens interstitial space, and progressive tubulointerstitial fibrosis. (Hu at el 2013) According to Clarkson and company, the presence of calcium oxalate crystals in the urine suggest a some kind of kidney obstruction, this may be explain the reason as to why there is a huge level of urea in her blood serum and the calcium oxalate crystals underlying acute kidney injury. She may experience excessive bleeding, she lost her conscious, has hematoma that is the accumulation of blood under the skin, which is an indicative of the presence of an elevated serum potassium. Her hand was broken and infected because of the poor blood circulation and high level of urea that causes itching resulting to her broken skins. (Clarkson et al 2008) WHAT OTHER TESTS COULD F2 CARRY OUT TO STRENGTHEN HER DIAGNOSIS As Bellomo and group, indicated that the diagnosis of acute kidney injury suggested that the renal dysfunction begins long before any detectable sufficient loss of excretory kidney function in standard laboratory tests. This is because urea and creatinine are insensitive markers of glomerular filtration rate and are may be modified by nutrition change, steroids use, presence of gastrointestinal blood, muscle mass, age, gender, or muscle injury. (Bellomo et al 2012) In addition, creatinine starts increasing only when there is more that 50% of is lost glomerular filtration rate, which could not be indicated on the trend of glomerular filtration rate and may be diluted after aggressive fluid resuscitation. (Macedo at el 2010) During acute kidney injury for any pathophysiologic consideration to take place, the sudden reduction in renal function usually occurs: because of that there is accumulation of creatinine and urea in the blood and there is a visible reduction of urine production. It has also been observed that both heart failure and kidney disease frequently occur together: heart insufficiency can be superimposed on acute kidney failure or chronic renal dysfunction or kidney disease may be linked to an acute or chronic decompensation cardiorenal and renocardiac syndromes. 5-10% of post-renal of acute kidney injury after nephron blood urea/creatinine ratio is equal to a normal range of 10:1. Even though the working condition of nephron is fine, the clinical indications are that urine cannot exit due to obstruction distal to kidney. This can be a result of: ureteric obstruction such as tumours, stones, and fibrosis, bladder cancer, or nephrolithiasis. (Ronco at el 2008) PHYSICAL EXAMINATION Assess whether she is dehydrated or fluid overloaded. Look for features of systemic disease, such as fever, skin rashes, joint swelling, or vascular disease. She has infected hands indicating that itching as a result of urea accumulation in the blood. Examine the abdomen for masses, abdominal aortic aneurysm and the bladder palpated and percussed for possible outflow obstruction. GLOMERULAR FILTRATION RATE The glomerular filtration rate is used to monitor acute kidney failure, which is the amount of blood filtered through all nephrons in one hour. Where 125cc/hr represents that normal glomerular filtration rate, if glomeruli are damaged, there is a decline of blood urea and creatinine filtration resulting in the accumulation of urea in the blood and elevated serum creatinine. (Cervi 2012) α-1 MICROGLOBULIN The α-1 microglobulin (α1M) is a protein that is synthesized in the liver and comprises of half circulated protein bound to IgA complex, which is filtrated by glomerulus and undergo reabsorption by proximal tubular cell. The α1M form with vast range of pH is stable in urine as found in routine clinical examination. It is preferred biomarker because of its sensitive biomarker for proximal tubular dysfunction, even for early stage of kidney dysfunction. (Vaidya et al 2008) N-ASETIL-β-GLUOSAMINIDASE (NAG) The N-asetil-β-glukosaminidase (NAG) is a lysosomal enzyme in proximal tubular, whose increase is a key diagnostic indicator and could identify patients who are at higher risk for GFR declining. It has been indicated in nephrotoxic drugs exposure, delayed renal allograft function, chronic glomerular disease, diabetic nephropathy, and it is also sensitive to detect acute kidney failure, which may precedes the increase of serum creatinine level by 12 hours to 4 days. (Makris at el 2009) INTERLEUKIN-18 (IL-18) The IL-18 is a pro-inflammatory cytokine which increased in endogenous inflammation process and was important in sepsis pathophysiology, pre-clinical observation suggests that IL-18 in urine has a potential as acute kidney injury. On the patients with acute kidney injury the level of IL-18 is elevated significantly in 24-48 hours prior to acute kidney injury. The IL-18 urine level increases 2 days earlier, which precedes the increase of creatinine level and has a sensitivity and specificity of >90% in diagnosing acute kidney injury and could be measured rapidly with ELISA method. (Washburn at el 2008) KIDNEY INJURY MOLECULE-1 The kidney injury molecule-1 (KIM-1) is a type 1 glycoprotein cell membrane, which contains domain resembling immunoglobulin called 6-cystein. The KIM-1 mRNA level in the blood is found to be elevated within a day or two after ischemic events following the acute kidney injury. The KIM-1 function in the kidney is to make epithelial cell be recognized by phagocytes to eliminate the dead cells caused by ischemia, which may result or contribute to obstruction that may have leads to acute kidney injury. The apoptosis of epithelial cell is expressed on the phosphatidylserine, which in turn is recognized by KIM-1 containing living cells and eliminated from the kidney. Thus, KIM-1 associated with epithelial cell works as phagocyte, therefore, urine level of KIM-1is increased in 12 hours after acute kidney injury, is highly specific and sensitive in identifying toxic substances in proximal tubular. (Bonventre 2009) RIFLE CRITERIA The need to describe acute kidney injury precisely and sensitively has caused development of a multidimensional of acute kidney damage classification system, which describes the severity of acute kidney failure. The most frequently used reference system is the RIFLE criteria (Risk, Injury, Failure, Loss, and End-stage Kidney Disease). RIFLE describes three severity stages of acute renal failure that is Risk, Injury and Failure and their two output variables that are Loss and End Stage Kidney Disease. The specific characteristics of the RIFLE classification include the presence of three variables to describe the severity of acute kidney failure based on serum creatinine level, glomerular filtration rate changes and its duration, and the severity of reduced urine production. The advantages of using RIFLE criteria is that we could establish diagnosis at the stage of preventable acute kidney failure, or when the renal injury has occurred, and the confirmed kidney failure. (Goldstein 2007) Reference list Bellomo R, Kellum JA, Ronco C. (2012) acute kidney injury. Lancet 380(9843) pp. 756-66. Bonventre JV. (2009)Kidney injury molecule-1 (KIM-1): a urinary biomarker and much more. Nephrol Dial Transplant. 1-4. Brincat S, Hilton R. (2008) acute kidney injury. GPonline, Cervi N J. (2012) acute kidney failure Documentation and coding CHIA Journal, pp. 6 Clarkson MR, Friedewald JJ, Eustace JA, Rabb H. (2008) acute kidney injury. In: Brenner BM, eds. Brenner and Rector’s The Kidney. 8th ed. Philadelphia, Pa: Saunders Elsevier; 29 Goldstein SL. (2007) Kidney function assessment in the critically ill child: Is it time to leave creatinine behind? Critical Care. (11)3 pp.141-2. Hilton R. (2006) Clinical review: acute renal failure. BMJ 333 pp. 786–90. Hu P, Wang J, Zhao XQ, Hu B, Lu L, Qin YH. (2013) Over expressed C-type natriuretic peptide serves as an early compensatory response to counteract extracellular matrix remodeling in unilateral ureteral obstruction rats. Mol Biol Rep. 40(2) pp. 1429-1441. Kanbay M, Kesapoglu B, Perazella MA. (2009) acute tubular necrosis and prerenal acute kidney injury: utility of urine microscopy in their evaluation-a systematic review. Int Urol Nephrol. 17. Lameire N, Van Biesen W, Vanholder R: (2006) The changing epidemiology of acute renal failure. Nat Clin Pract Nephrol, 2, pp. 364–377. Macedo E, Bouchard J, Soroko SH, Chertow GM, Himmelfarb J, Ikizler TA, Paganini EP, Mehta RL. (2010) Program to Improve Care in Acute Renal Disease Study. Fluid accumulation, recognition and staging of acute kidney injury in critically-ill patients. Crit Care. 14(3) pp. 82. Makris K, Markou N, Evodia E, Dimopoulou I, Drakoupoulos I, Ntetsika K, Rizos D. (2009) Urinary neutrophil gelatinase-associated lipocalin (NGAL) as an early marker of acute kidney injury in critically ill multiple trauma patients. Clin Chem Lab Med. (47)1 pp. 79-82 National Institute for Health and Clinical Excellence (NICE) (2008) Chronic kidney disease: Early identification and management of chronic kidney disease in adults in primary and secondary care. NICE. Segheb MM, Ghotbi SH, Moini M. (2008) Peripartum Acute Renal Failure. Shiraz E-Med J 9(1) pp. 45–54. Ronco C, House AA, Haapio M. (2008) Cardiorenal and renocardiac syndromes: the need for a comprehensive classification and consensus. Nat Clin Pract Nephrol. 4 pp. 310–1. Vaidya VS, Ferguson MA, Bonventre JV. (2008) Biomarkers of acute kidney injury. Ann Rev Pharmacol Toxicol. (48) pp. 463-93. Washburn KK, Zappitelli M, Arikan AA, Loftis L, Yalavarthy R, Parikh CR, Edelstein CL. (2008) Urinary interleukin-18 is an acute kidney injury biomarker in critically ill children. Nephrol Dial Transplant. (23) pp. 566-72. Read More